Head Trauma Flashcards by Louise Emerson

who are at high risk of head injuries

young men and elderly 
previous head injuries 
residents of inner cities
alcohol and drug abuse 
low income

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what do over half of head injuries involve

alcohol

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when do most deaths occur after head injury

within first hour
then peak at 7 hours- secondary effects
3rd peak later due to medical complications- high risk of pneumonia, DVT, PE

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what are the components of the glasgow coma scale

eye opening (4-1)

spontaneously
to speech
to pain
none

verbal (5-1)

orientated
confused
inappropriate
incomprehensible
no verbal

motor (6-1)

obeying
moves to localised pain
flexion withdrawal from pain
abnormal flexing (decorticate)
abnormal extension (decerebrate)
no motor response

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which part of glasgow coma scale carries most significance

motor

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what are the best and worst GCS scores

best 15

worst 3

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when is a patient comatosed on GCS

8 or less

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what are the parameters for head injury severity on GCS score

14/15, brief LOC= mild
9-13 = moderate
3-8= severe

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patients with what risk factors should have a CT scan done within 1 hour of being identified

GCS< 13 on initial assessment 
GCS< 15 2 hours after injury 
suspected open/ depressed skull fracture 
any sign of basal skull fracture
post traumatic seizure 
focal neurological deficit 
more than one episode of vomiting 
suspicion of NAI

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who should get a CT if they experienced some LOC or amnesia since the injury

> 65
coagulopathy (medically induced or thrombophilia)
dangerous mechanism of injury

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what does lacunar eyes mean

basilar skull fracture

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what is battles sign

bruising over the mastoid - basilar skull fracture

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what does any blood in CSF suggest

basilar skull #

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what is DAI (found in CT in diffuse head injury)

diffuse axonal injury

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what are the possible CT findings in a focal head injury

traumatic haemorrhage- extradural, subdural, intracerebral

contusion

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what are the features of an extradural haematoma

blood cant cross suture lines - fills space
lens shape/ biconvex shape
more common in younger patients

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what is the usual presentation of an extradural haematoma

injury with LOC
has lucid interval in recovery 
rapid progression of neurological symptoms 
-deteriorating GCS
-possible hemiparesis/ wekaness
-unilateral fixed and dilated pupil 
-apnoea and death

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what are the features of an acute subdural haematoma

more common in elderly
brain atrophy
bridging veins disrupted
will be hyPERdense

what will a chronic subdural haematoma look like on imaging

hyPOdense

what is an intracerebral haemoatoma

blood clot within the brain

what is coup and contra-coup

coup- brain hits side of head that is impacted

contra coup- brian hits opposite side

what causes a diffuse axonal injury

large shearing forces

what is the neurosurgical role in head injury

prevent secondary insults

hypoxia
hypotension
mass lesions
controlling ICP and CPP (cerebral perfusion pressure)

what formula calculated cerebral perfusion pressure

MAP - ICP

what maintains good cerebral perfusion pressure

maintained MAP (up) and ICP (down) at right levels

what are the basal cisterns

compartments within the subarachnoid space where the pia mater and arachnoid membrane are not in close approximation and cerebrospinal fluid (CSF) forms pools or cisterns mass have vessels/ nerves running through them

what does closure of the basal cisterns do

increases ICP

how is ICP monitored

wire inserted into head

what is the medical management for raised ICP

sedation- propofol, benzodiazepines, barbiturates maximise venous drainage of brain - head tilt of bed (30 degrees), cervical collars, ET tube ties co2 control osmotic diuretics - mannitol, hypertonic saline CSF release- external ventricular drain

how does CO2 affect ICP

if CO2 is too high cerebral blood flow increases- increasing ICP

what happens if arterial CO2 drops too low

reduce blood flow to brain by too much

what is a decompressive craniectomy and when is it done

after all medical management of raised ICP is exhausted take off part of cranium saves lives but doesnt improve outcomes

why do BP changes have such a big impact in head injury

as lose autoregulation, will directly impact cerebral blood flow

why is nutrition important in head injury

need to feed patients NG early on if not fed in 5-7 days after injury increase likelihood of death and mortality rate

why do axons swell up in DAI

as the injury (stretched, sheared, twisted or compressed) allows more ions and water into the axon

where do DAIs happen

where density difference is the greatest (grey/white interface)

what happens after DAI

excitotoxicity and apoptosis inflammatory mediator (cytokines, interleukins) response neuronal death

what is excitotoxicity

excitatory amino acids (gutamate) activates NMDA receptors calcium mediated activation of proteases and lipases cell death

do steroids help in head injuries

no- causes toxic swellings

what symptoms and signs suggest brainstem death

``` no pupil response no corneal reflex no gag reflex no vestibulo-ocular reflex (project cold water into one ear and look at eye movement) no motor response no respiration ```

what is the apnoea test

to look for brainstem death | Pre-oxygenate to look for a change in Co2 levels. Disconnect the ventilator and check pCO2 which must rise to 6 pKa

what are the possible long term complications of a head injury

``` Seizures Depression Alcohol and drug dependence Personality change Mood swings Aggression Recurrent behaviour – further head injuries Failure of relationships Loss of job suicide ```

what is ATLS

advanced trauma life support - airway with C spine control - breathing - circulation